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Fetal pain remains a controversial subject both in terms of recognizing its existence and the time-frame within which it appears. This article investigates the hypothesis that pain perception during development is not related to any determined structures of the central nervous system (CNS), on the contrary, the process of perception could be made with any structure satisfying conditions that the perception of pain is the organization, identification, and interpretation of sensory information in order to represent and understand the environment. According to this definition, chronic decerebrate and decorticate experimental animals, anencephalic, and hydranencephalic patients demonstrate that the basic, most general, appropriate interaction with the environment can be achieved with a functional mesodiencephalon (brain stem, and diencephalon) as the hierarchically highest structure of the CNS during development. In intact fetuses, this structure shows signs of sufficient maturation starting from the 15th week of gestation. Bearing in mind the dominant role of the reticular formation of the brain stem, which is marked by a wide divergence of afferent information, a sense of pain transmitted through it is diffuse and can dominate the overall perception of the fetus. The threshold for tactile stimuli is lower at earlier stages of gestation. The pain inhibition mechanisms are not sufficiently developed during intrauterine development, which is another factor that leads to increased intensity of pain in the fetus. As a conclusion it could be proposed that the fetus is exposed to rudimentary painful stimuli starting from the 15th gestation week and that it is extremely sensitive to painful stimuli.

The cerebellum, even when not directly damaged, is potentially interesting for understanding the adaptive responses to brain injury. Cerebellar electrocortical activity (ECoG) in rats was studied using spectral and fractal analysis after single and repeated unilateral injury of the parietal cortex. Local field potentials of cerebellar paravermal cortex were recorded before brain injury, in the acute phase (up to 2.5 hours) after a first injury of anesthetized rats, and then before and after second, third, and, in some cases, fourth injury. Relative gamma power (32.1-128.0 Hz) and fractal dimension of ECoGs were temporarily increased after the first injury. However, there was a permanent mild increase in gamma activity and a mild increase in the fractal dimension of cerebellar activity as a chronic change after repeated remote brain injury. There was a negative linear correlation between the normalized difference in fractal dimensions and normalized difference in gamma powers of cerebellar activity only in the case of repeated brain injury. This is the first study showing that correlation between the parameters of spectral and fractal analyses of cerebellar activity can discriminate between single and repeated brain injuries, and is, therefore, a promising approach for identifying specific pathophysiological states.

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Humans and guinea pigs are unable to produce vitamin C, with deficiency resulting in a well-known disorder of collagen synthesis. Pial basement membrane structure preservation is essential in the proper migration of neurons. In our study, intrauterine deprivation of vitamin C in guinea pig fetuses led to a collagen synthesis disorder, weakness, and finally a breach of pial basement membrane. We found excessive migration of the external germinal layer cells into the subarachnoid space of the cerebellum through defects in the pial basement membrane. The changes ranged from focal rupture of pial basement membranes to their complete disintegration. The loss of proper folia formation resulted in macroscopically visible flattening of the cerebellar surface. Different grades of dysplastic changes in the folia of the cerebellar cortex were observed in 2 experimental groups assigned different limits to mark the time of commencement and duration of vitamin C deprivation. The most severe form of dysplastic changes was characterized by marked irregularity of the cerebellar cortex similar to that in lissencephaly type II. Thus, prenatal vitamin C deficiency represents a novel animal model to study the effects of collagen synthesis on development of breaches in the pial basement membrane, disordered migration of neurons, dysplasia of cerebellar cortex, and the pathogenesis of lissencephaly.Keywords scurvy, cerebellum, guinea pigs, vitamin c deficiency, lissencephaly, animal model Lissencephaly type II is a disease caused by alteration to the pial basement membrane (PBM) proteins, which causes it to weaken and become porous. This causes a deficiency of the glia limitans superficialis and radial glial cell connectivity. As a result, migrating neural cells pass through the pial gaps to form cell ectopia near the brain surface. This leads to loss of gyri and sulci, forming irregularities on the brain surface and a so-called cobbled formation, which is why lissencephaly type II is also sometimes called cobblestone lissencephaly. 9,34Based on the fact that the structural integrity of the PBM is necessary for proper migration of the neurons, 2 main approaches have been established for experimental modeling of lissencephaly type II. First, animal models with targeted inactivation of genes involved in membrane protein synthesis have been studied. The lack of these proteins, such as collagen, laminin, and others, causes the PBM to weaken and finally rupture. 13,16,17,25,43 The second approach uses chemical destruction of meningeal cells over the developing cerebellum through exposure to 6-hydroxydopamine (6-OHDA). The loss of glio-pial membrane allows for overmigration of neurons through the pial breaches into the subarachnoid space. 1,29,30 Collagen is one of the key structural units of the basement membrane, and its synthesis is dependent on vitamin C. Humans, monkeys, and guinea pigs are unable to synthesize vitamin C because of a lack of L-gulono-g-lactone oxidase. 27It is well known that a deficiency of vitamin C in guinea...

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